期刊
CURRENT BIOLOGY
卷 28, 期 20, 页码 3337-+出版社
CELL PRESS
DOI: 10.1016/j.cub.2018.08.048
关键词
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资金
- Research Council of Norway [250005, 234817]
- Sars International Centre for Marine Molecular Biology Research, 2013-2022
Classical non-homologous end joining (c-NHEJ), a fundamental pathway that repairs double-strand breaks in DNA, is almost universal in eukaryotes and involves multiple proteins highly conserved from yeast to human [1]. The genes encoding these proteins were not detected in the genome of Oikopleura dioica, a new model system of tunicate larvaceans known for its very compact and highly rearranged genome [2-4]. After showing their absence in the genomes of six other larvacean species, the present study examined how a dioica oocytes and embryos repair double-strand DNA breaks (DSBs), using two approaches: the injection of linearized plasmids, which resulted in their rapid end joining, and a newly established CRISPR Cas9 technique. In both cases, end joining merged short microhomologous sequences surrounding the break (mainly 4 bp long), thus inducing deletions larger than for the tunicate ascidian Ciona intestinalis and human cells. A relatively high frequency of nucleotide insertions was also observed. Finally, a survey of genomic indels supports the involvement of microhomologymediated repair in natural conditions. Overall, O. dioica repairs DSBs as other organisms do when their c-NHEJ pathway is experimentally rendered deficient, using another mode of end joining with the same effect as alternative NHEJ (a-NHEJ) or microhomology-mediated end joining (MMEJ) [5-7]. We discuss how the exceptional loss of c-NHEJ and its replacement by a more mutation-prone mechanism may have contributed to reshaping this genome and even been advantageous under pressure for genome compaction.
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